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1

Wydzielnicza funkcja tkanki tluszczowej

100%
Kochan Z., Karbowska J.
Postępy Biochemii
|
2004
|
tom 50
|
nr 3
256-271
2

Nutritional regulation of glycerol kinase gene expression in adipose tissue is associated with up-regulation of PPAR gama

100%
Kochan Z., Karbowska J.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
3

Mikrobiologiczny rozklad zabytkowych pergaminow

100%
Strzelczyk A., Karbowska J.
Postępy Mikrobiologii
|
1993
|
tom 32
|
nr 1-2
19-32
4
Content available remote

Role of adiponectin in the regulation of carbohydrate and lipid metabolism

100%
Karbowska J., Kochan Z.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 6
103-113
Adiponectin, an adipocyte-derived plasma protein, has been shown to play an important role in the regulation of fatty acid and glucose metabolism. Adiponectin enhances fatty acid oxidation both in skeletal and cardiac muscle as well as in the liver, thus reducing triglyceride content in these tissues. Moreover, it stimulates glucose uptake by skeletal and cardiac muscle, and inhibits glucose production by the liver; consequently decreasing blood glucose levels. This review focuses on the molecular mechanisms underlying adiponectin effects on carbohydrate and lipid metabolism in skeletal muscle, cardiac muscle and liver.
5

The effects of clofibrate, a PPARalfa agonist, on adiponectin and resistin gene expression in adipose tissue

100%
Karbowska J., Kochan Z.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
6

The involvement of PPAR-alpha and PPAR-gamma signalling in long-term changes in lipogenic enzyme gene expression, as observed in rat adipose tissue after food restriction

100%
Kochan Z., Karbowska J.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
7

The role of microorganisms in the decay of parchment

100%
Strzelczyk A. B., Karbowska J.
Acta Microbiologica Polonica
|
1994
|
tom 43
|
nr 2
8

Rola adiponektyny - bialka wydzielanego przez tkanke tluszczowa w zapobieganiu miazdzycy

81%
Karbowska J., Brzezinski M., Kochan Z.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
tom 57
|
nr 5
579-591
9

Regulation of adiponectin receptor gene expression in the liver by clofibrate

81%
Langowska M., Karbowska J., Kochan Z.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
10

Fizjologiczna oporność na leptynę

81%
Gogga P., Karbowska J., Meissner W., Kochan Z.
Medycyna Weterynaryjna
|
2016
|
tom 72
|
nr 10
Leptin is an adipose tissue-derived hormone whose circulating levels correlate with the amount of body fat stores. The main function of this adipokine is to regulate energy metabolism. By modulating the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus, leptin reduces appetite. It also increases energy expenditure, contributing to the decrease of body fat and body weight. Mutations in the leptin receptor gene or prolonged consumption of a high-fat diet may impair leptin action, leading to leptin resistance. Resistance to leptin can also be an adaptive response that occurs in seasonal animals and in pregnant mammals. Reversible insensitivity to the satiety signal of leptin promotes hyperphagia, which is essential for animals living in dynamic environments and experiencing seasonal variation in food availability, since it allows them to forage intensely when food is abundant and accumulate fat reserves necessary to survive periods when food is scarce. Moreover, leptin resistance and subsequent hyperphagia develop during pregnancy in order to meet the energy needs of the growing fetus. Physiological leptin resistance may be due to impaired transport of leptin across the blood-brain barrier and/or to decreased sensitivity of the hypothalamus to this hormone resulting from an inhibition of leptin signalling in hypothalamic neurons. In pregnancy, an increased resistance to leptin action is also mediated by the binding of this adipokine to its placenta-derived soluble receptor. Reduced entry of leptin into the brain as well as alterations in the leptin signalling pathway in the hypothalamus leads to a transient decrease in sensitivity to this hormone preventing appetite suppression.
11
Content available remote

The effects of weight cycling on serum leptin levels and lipogenic enzyme activities in adipose tissue

81%
Kochan Z., Karbowska J., Swierczynski J.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 6
115-127
Weight cycling is one of the widely used weight reduction strategies; however, the adverse effects of this method include regaining significant amounts of weight. The molecular mechanisms underlying weight gain following cycles of dietary deprivation and refeeding are still poorly understood. One of the possibilities is that repeated loss and gain of weight may promote fat deposition in adipose tissue. To test this hypothesis we investigated serum leptin levels and lipogenic enzyme activities in white adipose tissue (WAT) of male Wistar rats during 12 days of ad libitum feeding following multiple cycles of alternating food deprivation and refeeding. Rats subjected to eight cycles of food deprivation and refeeding (MFR group) showed significantly decreased circulating leptin levels when compared with control rats (nearly 50% decrease in leptin levels, P < 0.01). Throughout 12 days of ad libitum feeding, serum leptin levels increased modestly but remained significantly (24%, P < 0.05) lower than control levels. Fatty acid synthase (FAS) and malic enzyme (ME) activities (chosen as representatives of enzymes directly involved in fatty acid synthesis) were found to be considerably higher in WAT of MFR rats refed for 3 days in comparison to control rats, and remained elevated even after 12 days of refeeding. These observations suggest that the elevation of lipogenic enzyme activities induced by multiple cycles of dietary deprivation followed by refeeding persists for several days, markedly increasing the lipogenic capacity of adipose tissue, which, accompanied by a decrease in circulating leptin levels, may promote weight gain.
12

Geny otylosci

81%
Swirszczynski J., Kochan Z., Karbowska J.
Postępy Biochemii
|
1997
|
tom 43
|
nr 3
174-181
13

Biologia molekularna i jej zastosowanie w medycynie

81%
Swierczynski J., Kochan Z., Karbowska J.
Kosmos
|
1997
|
tom 46
|
nr 1
17-24
14

The decrease in PPAR-alpha signalling in the failing human heart - a possible explanation for energy substrate preference switch

80%
Karbowska J., Kochan Z., Smolenski R. T.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
15

Peroxisome proliferator-activated receptor alpha is downregulated in the failing human heart

80%
Karbowska J., Kochan Z., Smolenski R. T.
Cellular and Molecular Biology Letters
|
2003
|
tom 08
|
nr 1
Cardiac hypertrophy in humans is associated with a decrease in myocardial fatty acid β-oxidation (FAO) and accompanying alterations in metabolic gene expression. Flux through the cardiac FAO pathway, which is the principal source of energy production in the adult mammalian heart, is tightly controlled in accordance with energy demands. In rodents, the FAO pathway is under control of a nuclear peroxisome proliferator-activated receptor α (PPARα). We sought to delineate the molecular regulatory events involved in the energy substrate preference switch from fatty acids to glucose during cardiac hypertrophic growth in humans. We analysed the amount of PPARα protein in human cardiac tissue. PPARα protein level was measured in homogenates prepared from left ventricular biopsies taken from five control donor hearts and compared to the amount of this transcription factor in biopsies from five patients with compensated end-stage heart failure (HF) at the time of transplantation. Using Western blot analysis with a monoclonal antibody against human PPARα, we observed a significant decrease (54%) in the mean amount of PPARα in the group of HF patients compared to that in the donor tissue. This study indicates that the decrease in cardiac PPARα transcription factor gene expression observed in the failing human heart could play an important role in a reduction in fatty acid utilisation by the adult heart during cardiac hypertrophy.
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